Sprague-Dawley rats were addicted to alcohol using a liquid diet supplemented with ethanol by means of intubation. The rats were sacrificed at various times after ethanol treatment and their blood, spleen, and thymus examined for numbers of lymphocytes and the ability of the lymphocytes to respond to non-specific T-cell and B-cell mitogens (cell proliferation stimulators). Lewis, as well as Sprague-Dawley, rats were immunized with sheep red blood cells prior to ethanol treatment and their ability to respond to an immunization by producing antibodies to the sheep red blood cells during the period of ethanol administration was tested. Bone marrow cells were also examined to determine the effects of ethanol on the erythroid (red) and myeloid (white) cell progenitors. Pyrodixine (B6) was also added to the ethanol treated animals' diet to determine whether or not protection from the deleterious effects of ethanol occurred. Both Lewis and Sprague-Dawley rats showed an impaired ability to react to an immunization while being treated with ethanol. Serum corticosterone levels were determined in adrenalectomized as well as normal animals. Animals treated with ethanol showed a decrease in lymphocyte cell numbers in the peripheral blood, spleen and thymus and an impaired ability of the lymphocytes to respond to non-specific T-cell and B-cell mitogens. Corticosterone levels were increased in ethanol treated animals. Two corticosterone peaks were seen - one after two days of intubation and the other on the day of withdrawal. Seven days after the end of ethanol treatment the rat lymphocytes approached control levels with regards to cell numbers and function. Ethanol treatment caused a decrease in marrow cellularity and a preferential decrease in colony growth in the erythroid cell line that was partially reversed by pyridoxine. Further investigations of possible contributing mechanisms of alcohol induced changes in the immune system are in progress.